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Table 2 Lipidomics data from plasma samples of patients

From: How does hepatic lipid accumulation lead to lipotoxicity in non-alcoholic fatty liver disease?

References Year Study cohort Technique Main findings
[47] 2009 Normal (n = 50)
NAFL (n = 25)
NASH (n = 50)
TLC 1. The total plasma MUFAs, which were driven by palmitoleic (16:1) and oleic (18:1) acids, were significantly increased in NAFL and NASH
2. The total SFAs were higher in both NAFL and NASH compared with control
3. The levels of DG and TG were significantly lower in NAFL and NASH compared with control
4. The total n-3 and n-6 PUFAs content progressively decreased in most lipid classes (including FFAs, TG, PC, LyPC)
5. Linoleic acid (8:2) was decreased with a concomitant increase in γ-linolenic (18:3) and dihomo γ-linolenic (20:3) acids in both NAFL and NASH
6. The plasma levels of AA (prostaglandin [PG]-M, PGB2, PGD2, PGE2, PGF2, and thromboxane A2) were not significantly different among normal, NAFL and NASH
7. The plasma levels of several products of the LOX pathway (5-HETE, 8-HETE, and 15-HETE) were significantly higher in NASH compared with NAFL/normal
[44] 2015 Normal (n = 31)
Steatosis (n = 17)
NASH (n = 20)
Cirrhosis (n = 20)
LC–MS 1. The plasma levels of several eicosanoids and FFAs were increased, whereas the plasma levels of many plasma neutral lipids, GPLs, and some sterols were reduced in cirrhosis, but not in NASH
2. Cirrhotic patients demonstrated decreased plasma levels of most SMs, long-chain bases, and glycolytic/TCA cycle metabolites, while increased plasma levels of several glucosylceramide species and nucleotides
3. NASH patients exhibited elevated ceramides, dihydroceramides, and 1-deoxy-dihydroceramides and 1-deoxy-ceramides
4. CEs, some sphingolipids and GPLs (e.g. PUFA PEs and those containing ether-linked moieties were increased), and the aqueous metabolite F16BP could distinguish NASH from steatosis
5. Sphingolipids and GPLs, which provide the best clustering by linear discriminant analysis, could distinguish all the histological states
[48] 2016 Non-NAFLD (n = 132)
NAFL (n = 117)
NASH (n = 69)
UPLC-MS 1. NASH was significantly associated with the elevated concentrations of saturated and monounsaturated TGs in the serum
2. NASH exhibited significantly reduced levels of SMs and lyPC compared with other groups
3. The absolute concentrations of saturated and monounsaturated TGs were significantly increased in NASH compared with other groups
4. The levels of saturated and monounsaturated TGs were elevated in NASH compared with non-NAFLD, and was inversely correlated with the number of double bonds
[49] Focused on circulating phospholipids 2018 Normal (n = 28)
NAFL (n = 25)
NASH (n = 42)
LC–MS 1. Increased circulating PC and SM, while decreased PE in NAFL and NASH
2. NASH patients demonstrated elevated PE compared with NAFL subjects
3. LyPE was significantly decreased in NAFL and NASH compared with control
4. The levels of PI and plasmalogens were not significantly different among all groups
5. NAFLD patients with hypertension demonstrated higher amounts of circulating PC and SM than NAFLD patients without hypertension
6. Diabetic (n = 18) and non-diabetic NAFLD patients (n = 49) showed no difference in the total phospholipids, including PC, PE and SM
[46] Focused on mitochondr-ial lipids 2018 Control (n = 16)
NAFL (n = 10)
NASH (n = 32)
LC–MS Acylcarnitines were increased in NASH compared with control
  1. NAFL non-alcoholic fatty liver, TLC thin-layer chromatography, FC free cholesterol, CE cholesterol ester, PC phosphatidylcholine, CL cardiolipin, PUFAs SFAs: saturated fatty acids, MUFAs monounsaturated fatty acids, AA arachidonic acid, DHA docosahexanoic acid (22:6 n-3), DPA docosapentenoic acid (22:5 n-3), PE phosphatidylethanolamine, LyPC lysophosphatidylcholine, COX cyclooxygenase, PS phosphatidylserine, SM sphingomyelin, TCA cycle the citric acid cycle, LOX lipoxygenases, HETE hydroxyeicosatetraenoic acid, LyPE lysophosphatidylethanolamine, GPL glycerophospholipid, PI phosphatidylinositol, F16BP fructose-1,6-bisphosphate